Unilateral optic nerve section (ONS) in rats causes two interesting effects: i) In rats raised at 3 lux illuminance it reduces the susceptibility of the ONS-eyes to retinal light-damage; and ii) in rats raised at 200 lux it reduces the rhodopsin level in the ONS- eyes. We propose to study ONS effects in the following ways: Rhodopsin levels and light-damage will be studied together in all groups of rats raised in 3 intensities: 3,100 and 200 lux. The time courses of the loss of rhodopsin and the loss of light-damage susceptibility will be examined to try and determine a cause - and - effect relationship. Then, we shall determine the cellular means whereby the rhodopsin changes are brought about, whether by changes in rod outer segment (ROS) length, packing density of rhodopsin in ROS disks or by loss of rod cells. In order to determine whether ONS-surgery differentially affects a certain region of the rat retina (as preliminary results indicate) we shall study the distribution of rhodopsin across the retina with a microspectrophotometer. Finally, we shall test the hypothesis that retinal efferents from the rat brain are involved in both retinal light-damage and rhodopsin levels. Testing this hypothesis will require tracing of neural pathways and making brain lesions that mimic the effects of ONS surgery. The proposed experiments will describe "neural" components in retinal light- damage and in the regulation of rhodopsin levels of the rat eye.